Coordinate loss of glucocorticoid responsiveness by intestinal enzymes during postnatal development.
Jejunal sucrase is known to display glucocorticoid responsiveness from birth through day 17 but not beyond that age. The aim of the current study was to determine whether this abrupt loss of responsiveness was shared by maltase, lactase, and acid beta-galactosidase. Glucocorticoid concentrations were manipulated by both adrenalectomy (ADX) and by administration of cortisone acetate (CA). Surgery or treatment was performed on each day from 16--22 days of age. Maltase activity was reduced by ADX at day 18 and earlier and was increased by CA at days 16 and 17. There were no effects at later ages. Acid beta-galactosidase was increased by ADX only at day 18 and earlier and was decreased by CA only at day 16. Lactase activity was increased by ADX at all ages up to and including day 20 but was reduced by CA only at days 16 and 17. Thus, we conclude that loss of glucocorticoid responsiveness at a relatively early stage of development is a common feature of both brush-border and lysosomal enzymes of the small intestine.
D000302:Adrenal Cortex / Q000502:physiology; D000375:Aging; D000818:Animals; D003348:Cortisone / Q000494:pharmacology*; D005696:Galactosidases / Q000378:metabolism*; D005959:Glucosidases / Q000378:metabolism*; D007583:Jejunum / Q000201:enzymology*; D008247:Lysosomes / Q000201:enzymology; D008871:Microvilli / Q000201:enzymology; D051381:Rats; D000520:alpha-Glucosidases / Q000378:metabolism*; D001616:beta-Galactosidase / Q000378:metabolism*
D005696:Galactosidases; D005959:Glucosidases; D000520:alpha-Glucosidases; D001616:beta-Galactosidase; D003348:Cortisone